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Involvement of central serotonergic pathways in analgesia elicited by salmon calcitonin in the mouse
M I Colado1, M J Ormazabal, C Goicoechea
1Departamento de Farmacología, Facultad de Medicina, Universidad Complutense, Madrid, Spain.
Abstract:
The contribution of central serotonergic pathways to the analgesic activity induced by salmon calcitonin in the writhing test was investigated. Salmon calcitonin was administered to mice after lesioning of the ascending and descending serotonergic pathways by means of i.p. administration of p-chloroamphetamine (40 mg/kg, for 2 days) or p-chlorophenylalanine (300 mg/kg, for 3 days). The analgesic effect induced by salmon calcitonin at the doses of 10 and 20 IU/kg was not evident in mice previously treated with p-chloroamphetamine or p-chlorophenylalanine. However, the analgesic effect of salmon calcitonin 40 IU/kg was not significantly modified by p-chloroamphetamine or p-chlorophenylalanine pretreatment. Salmon calcitonin did not alter the depletion of 5-hydroxytryptamine (5-HT) and 5-hydroxyindoleacetic acid after p-chloroamphetamine or p-chlorophenylalanine administration. Similarly, this hormone did not change the NSD 1015-induced accumulation of 5-hydroxytryptophan or the tranylcypromine-induced accumulation of 5-HT. These results indicate that although salmon calcitonin does not influence the synthesis and metabolism of 5-HT, it does require the integrity of the serotonergic system in order to cause analgesia.
Insights
Salmon calcitonin
Area of Science:
- Neuroscience
- Pharmacology
- Pain Research
Background:
- Salmon calcitonin exhibits analgesic properties.
- The role of central serotonergic pathways in this analgesia is not fully understood.
Purpose of the Study:
- To investigate the contribution of central serotonergic pathways to salmon calcitonin-induced analgesia.
- To determine if the integrity of serotonergic pathways is necessary for salmon calcitonin's pain-relieving effects.
Main Methods:
- Lesioning of serotonergic pathways in mice using p-chloroamphetamine or p-chlorophenylalanine.
- Administration of salmon calcitonin at varying doses (10, 20, 40 IU/kg).
- Assessment of analgesic activity in the writhing test.
- Measurement of 5-hydroxytryptamine (5-HT) and its metabolites.
Main Results:
- Salmon calcitonin's analgesic effect was diminished at lower doses (10, 20 IU/kg) in mice with lesioned serotonergic pathways.
- Higher doses of salmon calcitonin (40 IU/kg) retained analgesic activity despite pathway lesions.
- Salmon calcitonin did not affect 5-HT synthesis or metabolism.
Conclusions:
- The analgesic effect of salmon calcitonin is dependent on intact central serotonergic pathways.
- Salmon calcitonin requires the serotonergic system to exert its pain-relieving action, particularly at lower effective doses.